Changes in duodenal tissue-associated microbiota following hookworm infection and consecutive gluten challenges in humans with coeliac disease.

A reduced diversity of the gastrointestinal commensal microbiota is associated with the development of several inflammatory diseases. Recent reports in humans and animal models have demonstrated the beneficial therapeutic effects of infections by parasitic worms (helminths) in some inflammatory disorders, such as inflammatory bowel disease (IBD) and coeliac disease (CeD). Interestingly, these studies have described how helminths may alter the intestinal microbiota, potentially representing a mechanism by which they regulate inflammation. However, for practical reasons, these reports have primarily analysed the faecal microbiota. In the present investigation, we have assessed, for the first time, the changes in the microbiota at the site of infection by a parasitic helminth (hookworm) and gluten-dependent inflammation in humans with CeD using biopsy tissue from the duodenum. Hookworm infection and gluten exposure were associated with an increased abundance of species within the Bacteroides phylum, as well as increases in the richness and diversity of the tissue-resident microbiota within the intestine, results that are consistent with previous reports using other helminth species in humans and animal models. Hence, this may represent a mechanism by which parasitic helminths may restore intestinal immune homeostasis and exert a therapeutic benefit in CeD, and potentially other inflammatory disorders.

[Blastocystis hominis in symptomatic celiac patients]. / Blastocystis hominis en pacientes celíacos sintomáticos.

INTRODUCTION: Celiac disease (EC) not diagnosed or treated affect histological, immunological and nutritional status of patients who suffer it. These changes allow infection by parasites that cause no symptoms in immunocompetent patients, such as Blastocystis hominis (Bh). OBJETIVE. To analyze the presence of Bh in symptomatic celiac patients and describe the clinical, histological, immune and nutritional status in these patients. MATERIAL AND METHOD An observational descriptive cross sectional study was performed. Thirty symptomatic celiac patients (18 women, mean age 41 years old, range 19-68 years), assisted at the Institute of Gastroenterology of Cuba from January to December 2009, entered the study. RESULTS: Diarrhea and chronic anemia were the most commonly reported clinical manifestations (22 and 4 patients, respectively). The analysis of more than five Bh per field was more frequent in the group ofpatients studied (63.3%), with statistically significant difference in patients with vilous atrophy and low weight (P < 0.03) compared to cases with less than five Bh per feld. No significant differences were found when the immune status of patients was analyzed. CONCLUSIONS. In symptomatic celiac patients with subtotal-total villous atrophy and low weight the finding of more than five Bh perfield should be considered as opportunistic.

Celiac disease and giardiasis: a case report.

When investigating a patient with suspected celiac disease (CD), several other conditions must be considered, including potential infection with Giardia lamblia. Although giardiasis is rare, its histopathological and serological picture may resemble that of CD. We report the case of a young man with diabetes mellitus and a family history of CD referred to our hospital because of diarrhoea and weight loss. Investigation showed, among other factors, partial villous atrophy in duodenal biopsies and elevated immunoglobulin A antitissue transglutaminase antibodies. The patient was diagnosed with CD and recommended a gluten-free diet. At the same time, faecal tests were conducted, indicating the presence of G. lamblia. The patient was treated and improved, even after discontinuing the gluten-free diet. Subsequent follow-up after 6 months showed total regression of mucosal histopathology and a normal antitissue transglutaminase antibodies level.

Suppression of inflammatory immune responses in celiac disease by experimental hookworm infection.

We present immunological data from two clinical trials where the effect of experimental human hookworm (Necator americanus) infection on the pathology of celiac disease was evaluated. We found that basal production of Interferon- (IFN-)γ and Interleukin- (IL-)17A from duodenal biopsy culture was suppressed in hookworm-infected participants compared to uninfected controls. Increased levels of CD4+CD25+Foxp3+ cells in the circulation and mucosa are associated with active celiac disease. We show that this accumulation also occurs during a short-term (1 week) oral gluten challenge, and that hookworm infection suppressed the increase of circulating CD4+CD25+Foxp3+ cells during this challenge period. When duodenal biopsies from hookworm-infected participants were restimulated with the immunodominant gliadin peptide QE65, robust production of IL-2, IFN-γ and IL-17A was detected, even prior to gluten challenge while participants were strictly adhering to a gluten-free diet. Intriguingly, IL-5 was produced only after hookworm infection in response to QE65. Thus we hypothesise that hookworm-induced TH2 and IL-10 cross-regulation of the TH1/TH17 inflammatory response may be responsible for the suppression of these responses during experimental hookworm infection.